Pregnancy-Related Hypertension

How to Cite This Chapter: Gundy S, Naden R, Huynh A, Sułowicz W, Stompór T. Pregnancy-Related Hypertension. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed July 15, 2024.
Last Updated: October 4, 2021
Last Reviewed: October 4, 2021
Chapter Information

Etiology and PathogenesisTop

During pregnancy the maternal cardiovascular system undergoes several major physiologic changes. As early as 8 weeks’ gestation, peripheral vasodilatation can lead to a fall in systemic vascular resistance. To mitigate this effect, maternal cardiac output steadily increases, reaching upwards of 50% above the prepregnancy levels by weeks 20 to 24. As there is usually a lag in compensation, maternal blood pressure often falls slightly, by <5 mm Hg of systolic blood pressure (SBP), reaching a nadir around 20 to 22 weeks’ gestation before slowly rising back up to prepregnancy levels by term. After delivery, blood pressure may transiently decrease before peaking after 3 to 5 days.

Despite these physiologic changes, hypertension is one of the most common medical problems encountered in pregnancy. Complicating 5% to 10% of all pregnancies, certain etiologies are associated with significant maternal and fetal morbidity and mortality, requiring prompt identification, intervention, and management.


Classification of hypertension in pregnancy:

1) Preexisting hypertension: Chronic hypertension diagnosed before pregnancy or hypertension occurring before 20 weeks’ gestation. It may also present as persistent hypertension >3 to 6 months into the postpartum period.

a) Essential hypertension: No secondary cause identified.

b) Secondary hypertension (hypertension with an identifiable cause): Consider endocrine, renal, cardiac, or vascular abnormalities, depending on the clinical presentation.

2) Gestational hypertension: Hypertension identified after 20 weeks’ gestation without other features of preeclampsia; it may evolve into preeclampsia.

3) Preeclampsia: Hypertension occurring after 20 weeks’ gestation with proteinuria, end-organ dysfunction, or both.

a) De novo preeclampsia: New-onset hypertension and proteinuria or end-organ dysfunction.

b) Preexisting hypertension with superimposed preeclampsia: Worsening hypertension with new or worsening proteinuria or end-organ dysfunction.

c) Preexisting proteinuria with superimposed preeclampsia: New or worsening hypertension with worsening proteinuria or end-organ dysfunction; this is often due to chronic kidney disease, and the diagnosis of superimposed preeclampsia is complex. Involvement of a specialist in renal disease in pregnancy is advisable.


Blood pressure should be taken in a sitting rather than a supine position, as the gravid uterus may decrease venous return to the heart and produce abnormal increases or decreases in blood pressure. Measurements should be taken with a manual sphygmomanometer. Ensure the cuff size is appropriate for the patient so as not to overestimate the measurement (such as can occur with a cuff size too small). Phase V (disappearance) rather than phase IV (muffling) of Korotkoff sounds should be used.

The diagnosis of hypertension in pregnancy is made when the patient has at least 2 readings >140/90 mm Hg, taken in the office or hospital, measured at least 15 minutes apart. The severity of hypertension is based on BP readings and evidence of end-organ damage. Nonsevere hypertension is considered any BP between 140 to 159 mm Hg SBP and 90 to 109 mm Hg diastolic BP (DBP). Severe hypertension is defined as a BP ≥160/110 mm Hg.

Isolated office (white coat) hypertension may be revealed by home blood-pressure measurement. If there is any conflict between home and office readings, a 24-hour ambulatory blood-pressure monitor can be considered.

All patients with hypertension diagnosed before or during pregnancy should be followed closely by an obstetrician. Baseline blood tests to look for causes of secondary hypertension and exclude end-organ involvement should be ordered at the first visit at which hypertension is diagnosed.

The issue of when to search for a possible cause of secondary hypertension (see Essential Hypertension) is not always clear. The need for other tests may be prompted by the clinical features or clinical course. At a minimum, electrolytes, creatinine (estimated glomerular filtration rate), and urinalysis should be ordered. It is our practice to also obtain a complete blood count and liver function tests to use as a baseline or, in the case of patients at >20 weeks’ gestation, to exclude end-organ involvement from preeclampsia. Further information may be taken into account when judging the need for additional investigations (Table 1).

Management and TreatmentTop

General Approach

Regardless of the etiology of hypertension (preeclampsia, preexisting, gestational), the pharmacologic treatment of hypertension in pregnancy is approached in a similar manner. However, unlike the management of nonpregnant patients, the decision to treat hypertension must consider the risks and benefits to both mother and fetus. For this reason, the initiation of antihypertensive therapy should always be undertaken in consultation with an obstetrician. It is also vital to determine the etiology of the hypertension (primary, secondary, pregnancy-related) so that the clinical course and prognosis may be appropriately predicted.

1. General recommendations: Blood pressure levels, gestational age, and the presence of maternal and fetal comorbidities and complications must be taken into consideration.

1) Advise avoiding the supine position when lying down, as it may increase vasoconstriction.

2) Recommend maintaining a normal diet without salt restriction.

3) Normal physical activity need not be limited. Bed rest, unless in the setting of severely uncontrolled hypertension and/or severe preeclampsia, is not indicated.

2. Target blood pressure and levels at which to start antihypertensive treatment are controversial. On the one hand, maternal risk of cerebral hemorrhage increases with blood pressures >160/110 mm Hg; on the other, aggressive lowering of blood pressure may run the risk of compromising the uteroplacental blood supply due to reduced perfusion pressure into this largely passive vascular bed. Most clinicians will initiate treatment at levels >140 to 150 mm Hg SBP and >90 to 100 mm Hg DBP. A target DBP between 85 and 100 mm Hg in women with preexisting or pregnancy-induced hypertension (without preeclampsia) can be considered a safe zone for both mother and fetus. We suggest a target between 130 and 150 mm Hg SBP and 85 and 100 mm Hg DBP, recognizing that women with blood pressures closer to 150/100 mm Hg run an increased risk of developing severe hypertension and that slightly lower targets may also be reasonable.Evidence 1Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision and indirectness. The CHIPS trial indicated that there is no difference in maternal or fetal outcome between patients for whom the target diastolic blood pressure was <100 mm Hg (less tight) versus those whose target was <85 mm Hg (tight) except for a greater frequency of severe hypertension (>160/110 mm Hg) in the former group. All patients in the CHIPS trial had either preexisting hypertension or essential hypertension at enrolment. Magee LA, von Dadelszen P, Rey E, et al. Less-tight versus tight control of hypertension in pregnancy. N Engl J Med. 2015 Jan 29;372(5):407-17. doi: 10.1056/NEJMoa1404595. PubMed PMID: 25629739.

3. Treatment of nonsevere hypertension in pregnancy: First-line antihypertensive therapies include slow-release nifedipine, labetalol, or methyldopa (Table 2). These agents can be used alone or in combination as required. Second-line therapies (a fourth agent is rarely necessary) can include metoprolol, clonidine, hydralazine, or thiazide diuretics. Hydrochlorothiazide should be avoided if there is concern regarding a low amniotic fluid volume or in the setting of preeclampsia. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers are contraindicated.

4. Treatment of severe hypertension in pregnancy: Although there is a divergence in opinion regarding the optimal blood pressure cutoff at which to initiate medications and target treatment, a blood pressure of 160 mm Hg SBP or 110 DBP should always be treated. In such cases, both maternal and fetal well-being must be assessed and hospital admission considered. Medications including IV labetalol, oral short-acting nifedipine, or IV hydralazine can be used. Our preference is to use short-acting nifedipine, as it has been found to be as effective and safe as IV labetalol and does not require a parenteral route.Evidence 2Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision. Shekhar S, Sharma C, Thakur S, Verma S. Oral nifedipine or intravenous labetalol for hypertensive emergency in pregnancy: a randomized controlled trial. Obstet Gynecol. 2013 Nov;122(5):1057-63. doi: 10.1097/AOG.0b013e3182a9ea68. PubMed PMID: 24104790. Shekhar S, Gupta N, Kirubakaran R, Pareek P. Oral nifedipine versus intravenous labetalol for severe hypertension during pregnancy: a systematic review and meta-analysis. BJOG. 2016 Jan;123(1):40-7. doi: 10.1111/1471-0528.13463. Epub 2015 Jun 26. Review. PubMed PMID: 26113232. We prefer not to use hydralazine if other options are available. With all these drugs, small doses repeated every 30 to 40 minutes until the target blood pressure is reached are the safest regimen; this allows the full effect of each incremental dose to be seen and avoids overdose and an inappropriate reduction in perfusion pressure (all 3 of these drugs have an onset within 20 minutes and a peak effect within 40 minutes, whether given orally or IV). Of note, responses of individual patients to different drugs may differ significantly. Medication doses: Table 3.

5. Postpartum management: After delivery, maternal blood pressure often declines before rising once more between days 3 to 5 post partum, sometimes to levels higher than in pregnancy. Although this will often return to prepregnancy values within the following weeks, patients who have had a pregnancy complicated by hypertension may be particularly vulnerable to this postpartum surge, requiring an adjustment or addition of medication to prevent severe hypertension. All individuals with hypertension during pregnancy must be followed closely in the postpartum period. The use of nonsteroidal anti-inflammatory drugs for analgesia should be avoided, as it may aggravate hypertension. Any new or sudden worsening of hypertension with any associated signs and symptoms of end-organ dysfunction should prompt assessment for postpartum preeclampsia.

Antihypertensives used in pregnancy may be continued, as labetalol, slow-release nifedipine, and methyldopa are all considered safe in breastfeeding. However, ACEIs—particularly enalapril and quinapril—are both effective and safe and have the particular advantage that they have been shown not to cross into breast milk in an active form. Transition to prepregnancy medications may also be considered in the postpartum period.


Table 15.3-1. Screening for secondary causes of hypertension at initial assessment


Red flags

First-order testing


Evidence of renal impairment

Electrolytes (potassium)

Hypokalemia suggesting potential mineralocorticoid excess

Midstream urine

Evidence of proteinuria or hematuria suggesting a renal etiology

Urine PCR or 24-h urine collection for protein

If midstream urine is positive for proteinuria, recommend for baseline and quantitative assessment

Second-order testinga

Renal ultrasonography with Doppler

If sudden-onset or worsening hypertension, presence of abdominal bruit, resistance to ≥3 drugs, increase in serum creatinine ≥30% after using ACEI/ARB, significant asymmetry (>1.5 cm) in kidney size, recurrent pulmonary edema, significant atherosclerosis, family history of fibromuscular dysplasia, or personal history in another vascular territory

Sleep study

If evidence of sleep apnea in history (headache, nocturnal choking and gasping, early morning fatigue, snoring)

Plasma renin and aldosterone

If evidence of spontaneous hypokalemia (K <3.5 mmol/L) or hypokalemia with diuretics, resistance to ≥3 drugs, incidental adrenal adenoma

24-h urine metanephrines

If severe ≥180/110 mm Hg refractory hypertension, symptoms of catecholamine excess (headaches, palpitations, sweating, panic attacks, orthostatic syncope), hypertension triggered by beta-blockers, history of multiple endocrine neoplasia 2A or 2b, or incidental adrenal mass


If evidence of hypothyroidism or hyperthyroidism on clinical assessment

a Only undertaken if signs and symptoms present (see Essential Hypertension).

ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; PCR, protein-to-creatinine ratio; TSH, thyroid-stimulating hormone.

Table 15.3-2. Oral drugs for the management of hypertension in pregnancy


Starting dose

Maximum dose

Onset of action

Adverse effects

Special indications and notes


100 mg bid

500 mg qid

20‑40 min

Headache; avoid in uncontrolled asthma

Often requires tid or qid dosing in pregnancy; safe for breastfeeding

Nifedipine (slow release)

20 mg bid

60 mg bid

20‑40 min

Peripheral edema

Safe for breastfeeding


250 mg bid

1 g qid

1‑3 h

Fatigue; avoid in uncontrolled depression

Safe for breastfeeding

bid, 2 times a day; qid, 4 times a day; tid, 3 times a day.

Table 15.3-3. Drugs for the treatment of hypertensive emergencies in pregnancy



Onset/duration of action

Adverse effects

Special indication


20‑40 mg IV bolus every 20+ min

10‑20 min/3‑6 h

Vomiting, scalp tingling, burning sensation in the throat, dizziness, AV block

In most hypertensive emergencies except for acute heart failure

Nifedipine (short acting)

10 mg PO every 20+ min

10‑20 min/3‑6 h

Headache, facial flushing



5‑100 microg/min as IV infusion

2‑5 min/5-10 min

Headache, vomiting, methemoglobinemia, developing tolerance with prolonged use

Myocardial ischemia or pulmonary edema


10 mg IV bolus every 20+ min

10‑20 min/1‑4 h

Tachycardia, flushing, headache, vomiting, worsening of angina pectoris


AV, atrioventricular; IV, intravenous; PO, oral.

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